Necrotic complications
According to the revised Atlanta classification (revised Atlanta classification), acute pancreatitis is divided into two forms: interstitial edematous (interstitial oedematous) and necrotizing (necrotising). The necrotizing variant, in turn, manifests in three forms: combined pancreatonecrosis with peripancreatic necrosis (most common), isolated involvement of the peripancreatic adipose tissue, and isolated necrosis of the parenchyma itself.
In the early stages of the disease, an acute necrotic collection forms. Approximately 4 weeks after the onset of clinical manifestations, it matures, becoming demarcated from healthy structures by a thick connective tissue wall. This forms walled-off necrosis (Walled-Off Necrosis, WON). An important distinction between WON and a pseudocyst lies in its contents: the interior contains thick, unliquefied masses.
Infection of necrotic foci occurs in 20–70% of patients and is the leading cause of mortality (up to 80% of deaths from acute pancreatitis). Percutaneous drainage of such cavities with standard catheters often fails due to the high viscosity of the detritus. At the same time, modern data dictate moving away from immediate open necrosectomy: a conservative approach significantly reduces mortality—from 45% to 8.3%. Surgical intervention today is reserved exclusively for patients with intra-abdominal complications refractory to medical management.
Abscesses and pseudocysts
In interstitial edematous pancreatitis, an acute peripancreatic fluid collection initially forms. After 4 weeks, it can evolve into a pseudocyst (pseudocyst).
Pancreatic abscess is considered a relatively rare complication (observed in approximately 3% of patients with severe disease). Most often, it represents a pus collection arising secondary to the infection of a pseudocyst. According to diagnostic imaging, the most reliable sign of abscess formation is gas bubbles within the cavity. However, on CT, an abscess often simply looks like a fluid collection with a thick capsule, making its visual differentiation from sterile formations extremely difficult.
For an accurate diagnosis, the radiological picture must be correlated with clinical symptoms and inflammatory markers (C-reactive protein level, leukocytosis). If the abscess is clearly localized, contains no thick necrotic detritus, and infection is confirmed by fine-needle aspiration biopsy (FNA), percutaneous catheter drainage is indicated.
Vascular complications
The aggressive action of pancreatic enzymes, as well as mechanical compression by growing pseudocysts, frequently lead to erosion or thrombosis of adjacent major blood vessels.
- Venous system: The splenic vein is the most vulnerable. Its thrombosis can result in splenic infarction or massive intra-organ hemorrhage.
- Arterial system: Enzymatic damage to the wall of the splenic or gastroduodenal artery often leads to the formation of pseudoaneurysms. Their spontaneous rupture causes life-threatening internal bleeding (including directly into the pseudocyst cavity).
Contrast-enhanced computed tomography effectively identifies the source of the problem (e.g., contrast extravasation) and the localization of the pseudoaneurysm. In active bleeding, selective digital subtraction angiography (DSA) with subsequent microcoil embolization of the affected vessel (coil embolisation) is increasingly becoming the method of choice.
GI involvement and CT predictors of mortality
Due to close anatomical proximity, the inflammatory process easily spreads to the intestinal loops and stomach. This can lead to edema, necrosis, and even perforation of their walls. Secondary bowel involvement can also provoke vascular disorders leading to bowel ischemia.
Sometimes a spontaneous rupture of a walled-off necrotic collection into the digestive tract lumen occurs. In this case, gas appears in the necrotic zone, which can be mistakenly interpreted on tomograms as a sign of anaerobic infection.
CT signs reliably correlating with high mortality:
- Spread of the necrotic zone to more than one anatomical division of the gland (head, body, or tail) extending into adjacent tissues.
- Appearance of distant fluid collections—in the posterior pararenal space or along the paracolic gutters (paracolic gutter).
For quick memorization of collection outcomes after 4 weeks: Edema leads to a Pseudocyst (E-P), while Necrosis leads to Walled-off necrosis WON (N-W).
Class and exam questions
How to distinguish sterile necrosis from infected necrosis based on CT data?
The main radiological sign of infection is the presence of gas bubbles inside the collection. If imaging data are equivocal, fine-needle aspiration is performed (however, the procedure carries the risk of introducing bacteria into an initially sterile environment).
When is open surgery (necrosectomy) indicated in pancreatic necrosis?
Currently, open necrosectomy is avoided due to high mortality. It is used only in patients with concomitant intra-abdominal complications that do not respond to conservative therapy.
Why might percutaneous drainage of infected necrosis be ineffective?
Unlike an abscess or pseudocyst, the cavity of walled-off necrosis (WON) is filled with thick, unliquefied masses and detritus, which quickly clog the lumen of standard drainage catheters.
How is pseudoaneurysm bleeding treated in pancreatitis?
The gold standard for diagnosis and minimally invasive treatment is angiography followed by embolization of the damaged vessel (e.g., using coils).
What else to study on this topic
- Revised Atlanta classification of acute pancreatitis
- Differential diagnosis of pseudocysts and walled-off necrosis (WON)
- Indications and risks of fine-needle aspiration biopsy (FNA) in pancreatitis
- Mechanisms of pseudoaneurysm formation in enzymatic autolysis
- Angiography and embolization technique in vascular complications
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